ESC Heart Failure最新文献

{"title":"Long-term cardiovascular outcomes of immune checkpoint inhibitor-related myocarditis: A large single-centre analysis.","authors":"Lorenzo Braghieri, Ahmad Gharaibeh, Lubika Nkashama, Abdelrahman Abushouk, Osama Abushawer, Amir Mehdizadeh-Shrifi, Bianca Honnekeri, Cassandra Calabrese, Venu Menon, Pauline Funchain, Patrick Collier, Diego Sadler, Rohit Moudgil","doi":"10.1002/ehf2.15131","DOIUrl":"https://doi.org/10.1002/ehf2.15131","url":null,"abstract":"<p><strong>Aims: </strong>Immune checkpoint inhibitors (ICI) are the cornerstone of modern oncology; however, side effects such as ICI-related myocarditis (irM) can be fatal. Recently, Bonaca proposed criteria for irM; however, it is unknown if they correlate well with cardiovascular (CV) ICI-related adverse events. Additionally, whether incident irM portends worse long-term CV outcomes remains unclear. We aimed to determine the incidence of long-term CV comorbidities and CV mortality among irM patients.</p><p><strong>Patients and methods: </strong>The ICI-related adverse event (irAE) registry was queried to identify irM patients by using Bonaca criteria. Random controls were selected after excluding patients with other concomitant irAEs. Patients' demographics, comorbidities and myocarditis presenting features were gathered. Outcomes included 2-year freedom from CV comorbidities (composite of atrial fibrillation, stroke, myocardial infarction and heart failure) and freedom from CV death. IrM was treated as a time-varying covariate.</p><p><strong>Results: </strong>Seventy-six patients developed irM at a median of 167 days (mean age 69, 63.2% male, 47% lung cancer). Majority of patients had new wall motion abnormalities or EKG changes on presentation. Mean LVEF was 43%, median peak TnT was 0.81, and median NTproBNP was 2057 at irM onset. Two-year freedom from CV comorbidities (67% vs 86.8%, P < 0.001) and death (93.4% vs 99.3%, P = 0.003) was lower among irM patients. Incident irM was an independent predictor of CV death (HR 8.28, P = 0.048), but not CV comorbidities (HR 2.21, P = 0.080).</p><p><strong>Conclusions: </strong>This is the largest case-control study on irM highlighting worse long-term CV outcomes. Future studies are needed to establish appropriate therapeutic strategies and efficient screening strategies for irM survivors.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Iron deficiency in heart failure: Epidemiology, diagnostic criteria and treatment modalities.","authors":"Stephan von Haehling","doi":"10.1002/ehf2.15157","DOIUrl":"https://doi.org/10.1002/ehf2.15157","url":null,"abstract":"","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myocardial inflammation is associated with impaired mitochondrial oxidative capacity in ischaemic cardiomyopathy.","authors":"Julius Borger, Elric Zweck, Constanze Moos, Patrick Horn, Fabian Voß, Heinz-Peter Schultheiss, Jacob Eifer Møller, Udo Boeken, Hug Aubin, Artur Lichtenberg, Malte Kelm, Michael Roden, Amin Polzin, Ralf Westenfeld, Julia Szendroedi, Daniel Scheiber","doi":"10.1002/ehf2.15133","DOIUrl":"https://doi.org/10.1002/ehf2.15133","url":null,"abstract":"<p><strong>Aims: </strong>Myocardial inflammation and impaired mitochondrial oxidative capacity are hallmarks of heart failure (HF) pathophysiology. The extent of myocardial inflammation in patients suffering from ischaemic cardiomyopathy (ICM) or dilated cardiomyopathy (DCM) and its association with mitochondrial energy metabolism are unknown. We aimed at establishing a relevant role of cardiac inflammation in the impairment of mitochondrial energy production in advanced ischaemic and non-ischaemic HF.</p><p><strong>Methods: </strong>We included 81 patients with stage D HF (ICM, n = 44; DCM, n = 37) undergoing left ventricular assist device implantation (n = 59) or heart transplantation (n = 22) and obtained left ventricular tissue samples during open heart surgery. We quantified mitochondrial oxidative capacity, citrate synthase activity (CSA) and fibrosis and lymphocytic infiltration. We considered infiltration of >14 CD3⁺ cells/mm² relevant inflammation.</p><p><strong>Results: </strong>Patients with ICM or DCM did not differ regarding age (61.5 ± 5.7 vs. 56.5 ± 12.7 years, P = 0.164), sex (86% vs. 84% male, P = 0.725), type 2 diabetes mellitus (34% vs. 18%, P = 0.126) or chronic kidney disease (8% vs. 11%, P = 0.994). ICM exhibited oxidative capacity reduced by 23% compared to DCM (108.6 ± 41.4 vs. 141.9 ± 59.9 pmol/(s*mg), P = 0.006). Maximum production of reactive oxygen species was not significantly different between ICM and DCM (0.59 ± 0.28 vs. 0.69 ± 0.36 pmol/(s*ml), P = 0.196). Mitochondrial content, detected by CSA, was lower in ICM (359.6 ± 164.1 vs. 503.0 ± 198.5 nmol/min/mg protein, P = 0.002). Notably, relevant inflammation was more common in ICM (27% vs. 6%, P = 0.024), and the absolute number of infiltrating leucocytes correlated with lower oxidative capacity (r = -0.296, P = 0.019). Fibrosis was more prevalent in ICM (20.9 ± 21.2 vs. 7.2 ± 5.6% of area, P = 0.002), but not associated with oxidative capacity (r = -0.13, P = 0.327).</p><p><strong>Conclusions: </strong>More than every fourth ICM patient with advanced HF displays myocardial inflammation in the range of inflammatory cardiomyopathy associated with reduced mitochondrial oxidative capacity. Future studies may evaluate inflammation in ICM at earlier stages in standardised fashion to explore the therapeutic potential of immunosuppression to influence trajectories of HF in ICM.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of BMI with adherence and outcome in heart failure patients treated with wearable cardioverter defibrillator.","authors":"Mohammad Abumayyaleh, Katharina Koepsel, Julia W Erath, Thomas Kuntz, Norbert Klein, Boldizsar Kovacs, Firat Duru, Ardan M Saguner, Christian Blockhaus, Dong-In Shin, Fabienne Kreimer, Michael Gotzmann, Hendrik Lapp, Thomas Beiert, Assem Aweimer, Andreas Mügge, Christel Weiß, Ibrahim El-Battrawy, Ibrahim Akin","doi":"10.1002/ehf2.15141","DOIUrl":"https://doi.org/10.1002/ehf2.15141","url":null,"abstract":"<p><strong>Background: </strong>Obesity is a known risk factor for cardiovascular disease (CVD), yet an 'obesity paradox' has been observed in various CVD contexts. The impact of obesity on heart failure (HF) patients treated with a wearable cardioverter-defibrillator (WCD) remains underexplored.</p><p><strong>Methods: </strong>In a multicentre international registry, we retrospectively collected data from a consecutive series of 1003 patients. These patients were divided into three body mass index (BMI) groups: <25 kg/m² (n = 348), 25-30 kg/m² (n = 383), and >30 kg/m² (n = 272), with BMI > 30 kg/m² defined as the reference category. Demographics, indications, adherence, WCD shocks, arrhythmic events, rehospitalization due to cardiovascular causes, and mortality were analysed.</p><p><strong>Results: </strong>At 3 month follow-up, patients with a BMI > 30 showed the greatest improvement in left ventricular ejection fraction (LVEF) at 51.4%, significantly higher than the 41.4% in those with a BMI < 25 (P = 0.017) and comparable with the 49.4% in the BMI 25-30 group (P = 0.635). WCD wearing time and adherence were similar across all BMI groups. The incidence of WCD shock was similar across BMI groups. Rates of ventricular tachycardia (VT), ventricular fibrillation and non-sustained VT (ns-VT) were comparable across BMI groups. The rate of implantable cardioverter-defibrillator (ICD) implantation was 40.3% across all patients, with a slightly lower rate in the BMI > 30 group (36.8%) compared with others, although not significantly. Rehospitalization due to cardiovascular causes was significantly lower in the BMI > 30 group (55.4%) compared with the BMI 25-30 group (70.9%; P = 0.048), but similar to the BMI < 25 group (54.9%; P = 0.957). At 2 year follow-up, mortality was lower in the BMI > 30 group (5.9%) compared with the BMI < 25 (7.5%; P = 0.029) and BMI 25-30 groups (7%; P = 0.681). In multivariable analysis, LVEF at long term was significantly associated with a reduction in mortality.</p><p><strong>Conclusions: </strong>Obese patients exhibited significantly greater improvement in LVEF, which was associated with reduced mortality. Adherence to WCD therapy was excellent across all BMI groups. ICD implantation occurred in 40.3% of patients, with similar WCD shock rates and arrhythmic events across BMI groups. An obesity paradox was observed, with obese patients demonstrating significantly lower rehospitalization rates due to cardiovascular causes and reduced mortality at follow-up.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Left atrial function in uraemic patients: Four-dimensional automatic left atrial quantitative technology study.","authors":"Bing Li, Meihua Chen, Xuning Huang","doi":"10.1002/ehf2.15146","DOIUrl":"https://doi.org/10.1002/ehf2.15146","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to evaluate the utility of left atrial volume and function in uraemic patients using four-dimensional automatic left atrial quantification (4D auto LAQ) technology.</p><p><strong>Methods: </strong>Thirty-four undialysed uraemic patients (U-ND group), 60 dialysed uraemic patients (U-D group), and 32 healthy volunteers (N group) were enrolled in our current study. Conventional echocardiographic parameters were recorded, and left atrial volume and strain parameters were analysed to determine statistical differences among the three groups. The Pearson correlation coefficient was employed to assess the relationships between left atrial ejection fraction and left atrial strain parameters.</p><p><strong>Results: </strong>Compared to the N group, uraemic patients often displayed left atrial enlargement and left ventricular hypertrophy. Significant increases were noted in left atrial diameter, interventricular septum thickness, left ventricular posterior wall thickness, E/e', diastolic blood pressure, systolic blood pressure, left atrial minimum volume, left atrial maximum volume, left atrial pre-atrial contraction volume, left atrial emptying volume and left atrial maximum volume index (P < 0.05). Conversely, the e', E/A ratio and left atrial reservoir longitudinal strain were significantly decreased (P < 0.05). However, no statistically significant differences were observed in the aforementioned parameters between the U-ND and U-D groups. The absolute values of left atrial conduit longitudinal strain and left atrial conduit circumferential strain, as well as left atrial passive ejection fraction, were notably lower in the U-D group compared to the N and U-ND groups, with statistically significant differences identified among the three groups (P < 0.05).</p><p><strong>Conclusions: </strong>Uraemic patients exhibit marked left atrial enlargement and left ventricular hypertrophy, coupled with altered atrial function, particularly ductal dysfunction in the U-D group. The 4D auto LAQ technology proves advantageous in detecting these alterations, offering a promising tool for thorough cardiac assessment in this patient cohort.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Connecting the dots: A narrative review of the relationship between heart failure and cognitive impairment.","authors":"Mauro Massussi, Maria Giulia Bellicini, Marianna Adamo, Andrea Pilotto, Marco Metra, Alessandro Padovani, Riccardo Proietti","doi":"10.1002/ehf2.15144","DOIUrl":"https://doi.org/10.1002/ehf2.15144","url":null,"abstract":"<p><p>Large clinical data underscore that heart failure is independently associated to an increased risk of negative cognitive outcome and dementia. Emerging evidence suggests that cerebral hypoperfusion, stemming from reduced cardiac output and vascular pathology, may contribute to the largely overlapping vascular dementia and Alzheimer's disease. Despite these insights, cognitive outcomes remain largely overlooked in heart failure management. This narrative review outlines the prevalence and risk of cognitive impairment in heart failure patients, exploring potential shared pathophysiological mechanisms and examining the impact of heart failure therapy on cognitive deficits. Additionally, it discusses clinical implications and suggests future treatment approaches targeting therapeutic outcomes. Cognitive impairment is prevalent among individuals with heart failure, with reported rates varying widely depending on assessment methods. Shared pathological pathways and risk factors, including atrial fibrillation (AF), hypertension, obesity and type 2 diabetes mellitus, suggest a causal link. Mechanisms such as poor perfusion, microembolic events, ischaemic syndromes and cerebral inflammation contribute to this relationship. Moreover, heart failure itself may exacerbate cognitive dysfunction. This emerging understanding posits that vascular dementia and Alzheimer's disease may represent a pathophysiological continuum, driven by both the accumulation of misfolded proteins and cerebrovascular pathology due to cardiovascular dysfunction. Understanding these links is crucial for developing effective treatment strategies. The complex interplay between heart failure and cognitive impairment underscores the necessity for a holistic patient care approach. Both conditions share analogous disease processes, influencing self-management and independence in patients. Prioritizing brain health in heart failure management is essential to enhance patient prognosis and general well-being.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The in-hospital administration of sacubitril/valsartan in acute myocardial infarction: A meta-analysis.","authors":"Gianluca Di Pietro, Riccardo Improta, Paolo Severino, Andrea D'Amato, Lucia Ilaria Birtolo, Ovidio De Filippo, Antonio Lattanzio, Raffaele De Cristofaro, Giacchino Galardo, Fabrizio D'Ascenzo, Roberto Badagliacca, Gennaro Sardella, Maurizio Volterrani, Francesco Fedele, Carmine Dario Vizza, Massimo Mancone","doi":"10.1002/ehf2.15082","DOIUrl":"https://doi.org/10.1002/ehf2.15082","url":null,"abstract":"<p><p>There is a need to address the evidence gap regarding the in-hospital administration of sacubitril/valsartan in acute myocardial infarction patients. After searching MEDLINE, Google Scholars and Scopus, a random-effects meta-analysis of randomized controlled trials comparing the in-hospital administration of the angiotensin receptor-neprilysin inhibitors (ARNis) versus the standard therapy in patients with reduced heart failure due to myocardial infarction was performed. The primary outcome was major adverse cardiovascular events. All-cause mortality, cardiac death, rehospitalization for heart failure, non-fatal myocardial infarction (MI), changes in left ventricular ejection fraction, left ventricular volumes, N terminal pro brain natriuretic peptide and adverse events were the secondary endpoints. Nine studies (eight randomized controlled trials and one echo-substudy) with a total 6597 individuals (angiotensin-converting enzyme inhibitor/angiotensin receptor blocker: 3300 patients vs. ARNis: 3297 patients) were included for quantitative analysis. Median follow-up was 6 months. Patients receiving an in-hospital coadministration of ARNi had a lower risk of major cardiovascular event [odds ratio (OR) 0.45, 95% confidence interval (CI) 0.32-0.63, P < 0.0001] and lower rate of repeat rehospitalization for heart failure (OR 0.40, 95% CI 0.26-0.62, P < 0.0001), compared with a standard regimen. Additionally, left ventricle volumes were significantly lower in the ARNi group [left ventricular end-diastolic volume, mean difference (MD) 11.48 mL, 95% CI 6.10-16.85, P < 0.0001; left ventricular end-systolic volume, MD 7.09 mL, 95% CI 2.89-11.29, P = 0.0009] with a significant change in left ventricular ejection fraction (MD 3.07, 95% CI 1.61-4.53, P < 0.0001), compared with standard therapy. No significant differences were observed in terms of cardiac death, all cause of mortality, non-fatal myocardial infarction and N terminal pro brain natriuretic peptide. Higher rates of iatrogenic hypotensive events were observed in the ARNi group compared with the standard therapy (OR 1.42, 95% CI 1.26-1.60, P value < 0.00001). In patients with acute myocardial infarction related heart failure, the in-hospital administration of ARNis was associated with a reduced risk of major cardiovascular events and re-hospitalization for heart failure, as well as cardiac remodelling, but higher rates of hypotensive events compared with standard therapy.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased calcification by erythrophagocytosis in aortic valvular interstitial cells.","authors":"Zihan Qin, Magnus Bäck, Anders Franco-Cereceda, Sven-Christian Pawelzik","doi":"10.1002/ehf2.15132","DOIUrl":"https://doi.org/10.1002/ehf2.15132","url":null,"abstract":"<p><strong>Background: </strong>Calcific aortic valve disease (CAVD) progresses over time to severe aortic stenosis and eventually heart failure. Recent evidence indicates that intraleaflet haemorrhage (ILH) strongly promotes CAVD progression. However, it remains poorly understood how it mechanistically contributes to valvular calcification.</p><p><strong>Method: </strong>ILH was identified as iron deposition by morphological analysis. To elucidate the underlying mechanism, human valvular interstitial cells (VIC) were cultured in the presence of fresh or senescent red blood cells (RBC), simulating ILH in vivo conditions.</p><p><strong>Result: </strong>ILH was common in aortic valves derived from patients with severe aortic stenosis. VIC undergo erythrophagocytosis of senescent RBC, leading to intracellular iron accumulation analogous to observed following exposure to extracellular iron. The presence of senescent RBC significantly intensified VIC calcification, which was significantly mitigated by ferroptosis inhibition.</p><p><strong>Conclusions: </strong>Our results identify erythrophagocytosis by VIC, leading to iron accumulation and enhanced calcification through ferroptosis. This may be a crucial component of the pathophysiological mechanisms that links ILH to valvular calcification and accelerated aortic stenosis progression.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Considerations for drug trials in hypertrophic cardiomyopathy.","authors":"John P Farrant, Matthias Schmitt, Anna B Reid, Clifford J Garratt, William G Newman, Aneil Malhotra, Rhys Beynon, Masliza Mahmod, Betty Raman, Robert M Cooper, Dana Dawson, Thomas Green, Sanjay K Prasad, Anvesha Singh, Susanna Dodd, Hugh Watkins, Stefan Neubauer, Christopher A Miller","doi":"10.1002/ehf2.15138","DOIUrl":"https://doi.org/10.1002/ehf2.15138","url":null,"abstract":"<p><p>Hypertrophic cardiomyopathy (HCM) is a heterogeneous condition with potentially serious manifestations. Management has traditionally comprised therapies to palliate symptoms and implantable cardioverter-defibrillators to prevent sudden cardiac death. The need for disease-modifying therapies has been recognized for decades. More recently, an increasing number of novel and repurposed therapies hypothesized to target HCM disease pathways have been evaluated, culminating in the recent regulatory approval of mavacamten, a novel oral myosin inhibitor. HCM poses several unique challenges for clinical trials, which are important to recognize when designing trials and interpreting findings. This manuscript discusses the key considerations in the context of recent and ongoing randomized trials, including the roles of genotype, phenotype and symptom status in patient selection, the evidence base for clinical and mechanistic outcome measurements, trial duration and sample size.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic value of hypoxaemic burden from overnight oximetry in heart failure with preserved ejection fraction.","authors":"Sanne G J Mourmans, Jerremy Weerts, Mathias Baumert, Arantxa Barandiarán Aizpurua, Anouk Achten, Christian Knackstedt, Dominik Linz, Vanessa P M van Empel","doi":"10.1002/ehf2.15116","DOIUrl":"https://doi.org/10.1002/ehf2.15116","url":null,"abstract":"<p><strong>Aims: </strong>Nocturnal hypoxaemic burden, quantified as time spent with oxygen saturation below 90% (T90), is an established independent predictor of mortality in heart failure (HF) with reduced ejection fraction. The prognostic value of T90 in HF with preserved ejection fraction (HFpEF) is unknown. This study aims to determine the association of T90 with adverse outcomes in HFpEF.</p><p><strong>Methods and results: </strong>One hundred twenty-six patients prospectively included from our specialised HFpEF outpatient clinic underwent ambulatory home sleep monitoring to obtain oximetry data, including T90. We investigated the association between T90 and a composite endpoint of HF hospitalisations or all-cause mortality. Nocturnal hypoxaemic burden in this HFpEF population was high, with a median T90 of 13.7 min. In only 10 patients (7.9%), oxygen saturation was at no time point below 90%. After median 34 months [IQR 18.4-52.0] of follow-up, 32 patients (25%) reached the composite endpoint. T90 was significantly associated with the composite endpoint, also after adjusting for potential confounders (HR 1.004 (95% CI 1.001-1.007, P = 0.019) per 1 min T90 increase or HR 1.265 (95% CI 1.061-1.488) per 1 h T90 increase). Patients with HFpEF in the highest T90 tertile (T90 ≥ 31.4 min) had a significantly higher event rate compared to patients in the lowest two T90 tertiles, with 19 (45%) versus 13 (15%) events, respectively (P < 0.001).</p><p><strong>Conclusions: </strong>Nocturnal hypoxaemic burden is an independent prognostic marker for the composite of HF hospitalisations or all-cause mortality in HFpEF. Whether reduction of T90 improves the prognosis of patients with HFpEF warrants further research.</p>","PeriodicalId":11864,"journal":{"name":"ESC Heart Failure","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}